Dr. Bin Sun, a Dphil graduate from the Szele Research group within the Department, has published a paper in Cerebral Cortex based on his work.
Bin's research showed that an epigenetic modification - diminishing the multi-protein complex "polycomb repressor complex 2" (PRC2) - severely reduces SVZ neurogenesis. He showed that selectively removing extra embryonic development (Eed) affects the maintenance of stem cells in the SVZ. This was a different effect from when he removed the enhancer of zeste 2 (Ezh2) methyltransferase component of PRC2, which Bin showed works downstream in the SVZ lineage.
Based on the embryonic stem cell literature, Bin went on to hypothesize that Eed may normally suppress expression of the transcription factor Gata6 and showed that this indeed was the case. He demonstrated that Gata6 overexpression phenocopied loss of Eed and that knocking Gata6 down was sufficient to rescue Eed function. Gata6 can affect expression of a key cell cycle regulator called P21 (a cyclin-dependent kinase inhibitor). Bin elegantly showed that in the SVZ, Gata6 regulates not transcription of P21 but its post-translational stability.
Finally he showed that Eed is necessary for activating SVZ repair mechanisms in traumatic brain injury.
Thus, Bin has made several important novel discoveries that have bearing on our understanding of how adult neurogenesis is regulated.
Congratulations Dr Sun!
To find out more information about what the Szele Research group gets up to, visit their website page.